M2 Micro 20 Ex1

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Corynebacterium pseudodiphtheriticum Infections

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Respiratory tract infections
Pharyngitis, bronchitis, tracheitis, tracheobronchitis pneumonia, lung abscess in compromised hosts
Native- and prosthetic-valve endocarditis
Wound infections

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Corynebacterium pseudodiphtheriticum txt

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Susceptible to β-lactam agents, vancomycin, and aminoglycosides

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Corynebacterium jeikeium

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Lipophilic corynebacterial species that colonizes the skin of hospitalized patients

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Corynebacterium jeikeium Infections

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Immunocompromised hosts (malignancies/underlying diseases)
Infections of indwelling medical devices, barrier breaks,
Neutropenia patients on broad-spectrum agents
Community- and nosocomially acquired infections

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Corynebacterium urealyticum

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Found on the skin of humans and animals
Associated with acute and chronic UTI’s in elderly, compromised hosts, and animals (e.g., dogs)

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Corynebacterium urealyticum Infections

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Urolitiasis and alkaline-encrusted cystitis in those with pyelonephritis (struvite deposition)
Osteomyelitis, bacteremia, endocarditis, soft tissue and wound infections

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Corynebacterium urealyticum ID

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Urease-RAPIDLY POSITIVE!!! (minutes)
Asaccharolytic

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Corynebacterium urealyticum txt

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Quinolone susceptibility is variable
Susceptible to doxycycline, rfampin, and vancomycin

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Arcanobacterium haemolyticum

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Pharyngitis and wound infections in children and young adults
Often associated with a “scarlatinaform rash”
May be mistaken for group A streptococcal pharyngitis
“Direct Group A antigen” tests are NEGATIVE

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Bacillus spp feats

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Gram positive/variable rods
Facultative
Most grow better aerobically
Endospores formed under aerobic conditions
Catalase-positive
Cytochromes present
Many species
B. anthracis
B. cereus

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Virulence Factors of B. anthracis

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toxins
Structural genes (pagA, cya, and lef) reside on a plasmid (pX01

Another pXO1 gene (atxA) encodes a trans-acting regulatory protein that activates transcription of these structural genes

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B. anthracis toxins composed of 3 proteins

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Protective antigen (PA)
Edema factor (EF)
Lethal factor (LF)

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Protective antigen (PA)
PA is secreted, binds to target cell receptors,and undergoes

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proteolytic cleavage
Bound PA fragments aggregate to form ring-shaped hexamers that result in pores through the target cell membrane

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B. anthracis PA/EF complex = edema toxin (ET)
PA/LF complex = lethal toxin (LT)

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Inhibit phagocytosis
Blocks oxidative burst of PMNs
Increases intracellular cAMP levels

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In macrophages, LT:

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Inhibits macromolecular synthesis
Promotes apoptosis
Hydrolyzes protein kinases involved in intracellular signal transduction

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Capsule of Bacillus anthracis Genes reside on a second

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plasmid (pXO2)

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Bacillus anthracis Capsule is

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a polymer of γ-linked α-peptide chains of glutamic acid (50-100 residues)
Capsule inhibits phagocytosis
Capsule synthesis influenced by levels of CO2 and bicarbonate in vivo and in vitro

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B. anthracis infects mostly

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farm animals and usually spread to humans through a break in the skin

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Cutaneous Anthrax

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Most common form (95%)
Inoculation of spores under skin
Incubation period: Several hours to 7 days
Small papule that ulcerates, surrounded by vesicles (24-48 hours)
Painless eschar with edema
Mortality of 20% if untreated

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Oropharnygeal Anthrax

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Nine days after the onset of symptoms a white pseudomembrane has developed over the right tonsil, soft palate and uvula

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Gastrointestinal Anthrax

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Ingestion of contaminated meat
Incubation period of hours up to 7 days
Fever, acute gastroenteritis, vomiting, bloody diarrhea

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Gastrointestinal Anthrax Intestinal eschar similar to

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cutaneous anthrax lesion (hemorrhagic)

Progresses to generalized toxemia
Mortality of 50 to 100%

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Inhalational Anthrax

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Inhalation of spores

Initial symptoms:
2-5 days
Fever, cough, myalgia, malaise
Terminal symptoms:
1-2 days; high fever, dyspnea, hemorrhagic mediastinal widening with pleural effusions
Rapid progression to shock and death

PNEUMONIA NOT PART OF DISEASE PRESENTATION

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Once Inhalational Anthrax has reached the terminal phase

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theres no way to treat. The key to know it is anthrax is by a wide mediastinum

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Specimens for Isolation of Bacillus anthracis

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Swabs/biopsies from suspected eschars
Stool (may not yield the organism)
Blood
Hemorrhagic fluids from the nose, mouth, or anus
Aspirates from peritoneum, spleen, mesenteric lymph nodes
Paired serum specimens

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Bacillus anthracis: Sentinel Lab Tests

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Colony, 35oC
Non-hemolytic
“Ground glass”
“Egg white” consistency
“Medusa-head” margins

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Bacillus anthracis: feats

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Motility: Negative
Forms capsule:
India ink-Pos
Penicillin susceptible
β-lactamase-Neg

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B anthracis key lab feats that separate it from other bacillus

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Hemolysis negative
Motily negative
Hydrolysis of Gelatin Negative

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Identification of B. anthracis

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Capsule-Specific FA Stain (l) and Phage Lysis Test (r) slide 78

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Bacillus cereus Gastroenteritis Diarrheal Syndrome

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Heat-labile enterotoxin
Abdominal pain with watery diarrhea 8-16 hours after ingestion
Meat, vegetables, cakes, sauces, dairy products

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Bacillus cereus Gastroenteritis Emetic Syndrome

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Heat-stable enterotoxic dodecadepsipeptide (cerulide, MW = 5 kDa)
Nausea and vomiting 1-6 hours after ingestion
Oriental rice dishes, dairy products

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Infections Associated with Non-Anthrax Bacillus Species

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Primary bacteremia and endocarditis
Endophthalmitis following penetrating eye injuries (emergency because bug can destroy orbit of eye in matter of hrs)
Infections in compromised hosts
Musculoskeletal infections
Nosocomial infections and “pseudo-outbreaks

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Bacillus spp. NOT ANTHRAX
Produce

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β-lactamase

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Bacillus spp Susceptible to

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clindamycin, erythromycin, vancomycin, tetracyclines, and sulfonamides
Resistant to trimethoprim

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NocardiaNocardia

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Found in soil, deomposing vegetation, fresh and salt water

Beaded appearance with both Gram stain and modified acid-fast stain

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Risk Factors for Infection with Nocardia

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Lung transplant recipients at highest risk

Human stem-cell transplant (HSCT) patients
Allogeneic hematopoietic HSCT recipients at higher risk than those with autologous hematopoietic transplants
Development of GVHD accounts for some of the increased risk
May occur 2-3 months or up to 1-3 years after stem cell infusion
Corticosteroids or other immunosuppressive medications
COPD patients taking corticosteroids are at increased risk

HIV infection

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Clinical Presentations of Nocardiosis: Nocardia Pneumonia

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Pulmonary infection is the most common clinical presentation
Onset is subacute or chronic
Productive or non-productive cough
Shortness of breath
Chest pain
Fever, night sweats, weight loss, progressive fatigue

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Nocardiosis: Nocardia Pneumonia CXR

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Variable
Focal or multi-focal disease with a nodular or consolidated infiltrate
Cavitary lesions may be seen
Pleural effusion present in up to one-third of patients

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Pulmonary Nocardia Infection

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Multiple pulmonary nodules, demonstrated by computed tomography (A) and chest radiograph (B), in an immunosuppressed patient with disseminated nocardiosis.

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Extra-Pulmonary Nocardiosis

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CNS is the most common extra-pulmonary location (up to 44% in one case series)
One or more brain abscesses
Headache, nausea, vomiting, seizures, altered sensorium
Neurologic symptoms develop gradually
CNS disease usually accompanies pulmonary disease

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Nocardiosis Primary Cutaneous/Soft-Tissue Infection

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Traumatic injury to the skin in the presence of soil contamination (happens in people with little access to healthcare
Advanced Infections: Mycetoma with Sinus Tract Development

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Nocardia Species colonies smell like

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flooded basement

Waxy cerebriform colonies that develop a dry, chalky appearance when aerial hyphae are produced

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Nocardia spp. Modified Acid Fast Stain

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No other organism looks like these…he said..we shouldn’t miss It in atest.
96

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Agents Used to Treat Nocardia Infections

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Trimethoprim/Sulfamethoxazole